miR-335 Targets SIAH2 and Confers Sensitivity to Anti-Cancer Drugs by Increasing the Expression of HDAC3

Kim, Youngmi; Kim, Hyuna; Park, Deokbum; Jeoung, Dooil

doi:10.14348/molcells.2015.0051

Cited by 32 publications

(33 citation statements)

References 58 publications

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“…Moreover, the GO functional annotation analysis was performed and found that the four genes were annotated with drug responses related GO terms (Table S6), such as cell cycle, apoptotic process, and DNA damage response. In the STAD DRCEs, four lncRNA, RP11‐473O4.3, LINC01184, LINC00641, and ENSG00000248175, competed for binding to miR‐331, miR‐335, and miR‐106b, which are known to be associated with chemotherapy resistance (Feng et al ., 2011; Kim et al ., 2015; Xia et al ., 2008), thereby regulating their target genes. Consequently, the six DRCEs, hsa‐miR‐335_KLF8_LINC00641, hsa‐miR‐106b_APC_ENSG00000248175, hsa‐miR‐106b_APC_LINC01184, hsa‐miR‐106b_CCND2_ENSG00000248175, hsa‐miR‐331_ATRX_ENSG00000248175, and hsa‐miR‐331_ATRX_RP11‐473O4.3, may affect 5‐FU drug responses (Fig.…”

Section: Resultsmentioning

confidence: 99%

Inferences of individual drug responses across diverse cancer types using a novel competing endogenous RNA network

Zhang

Zhou

et al. 2018

Molecular Oncology

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Differences in individual drug responses are an obstacle to progression in cancer treatment, and predicting responses would help to plan treatment. The accumulation of cancer molecular profiling and drug response data provides opportunities and challenges to identify novel molecular signatures and mechanisms of tumor responsiveness to drugs. This study evaluated drug responses with a competing endogenous RNA (ceRNA) system that depended on competition between diverse RNA species. We identified drug response‐related ceRNA (DRCEs) by combining the sequence and expression data of long noncoding RNA (lncRNA), microRNA (miRNA), and messenger RNA (mRNA), and the survival data of cancer patients treated with drugs. We constructed a patient–drug two‐layer integrated network and used a linear weighting method to predict individual drug responses. DRCEs were found to be significantly enriched in known cancer and drug‐associated data resources, involved in biological processes known to mediate drug responses, and correlated to drug activity in cancer cell lines. The dysregulation of DRCE expression influenced drug response‐associated functions and pathways, suggesting DRCEs as potential therapeutic targets affecting drug responses. A further case study in breast invasive carcinoma (BRCA) found that DRCE expression was consistent with the drug response pattern and the aberrant expression of the two NEAT1‐related DRCEs may lead to poor response to tamoxifen therapy for patients with TP53 mutations. In summary, this study provides a framework for ceRNA‐based evaluation of clinical drug responses across multiple cancer types. Understanding the underlying molecular mechanisms of drug responses will allow improved response to chemotherapy and outcomes of cancer treatment.

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Section: Resultsmentioning

confidence: 99%

Inferences of individual drug responses across diverse cancer types using a novel competing endogenous RNA network

Zhang

Zhou

et al. 2018

Molecular Oncology

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“…Given the major roles of miRNAs in regulating protein expression in general, it is reasonable to infer that targeting miRNAs could be a promising approach to overcome drug resistance. A growing body of data indicates that miR-335 plays an essential role in drug resistance (25)(26)(27). Kim et al found that miR-335/SIAH2/HDAC3 axis regulates the response to anticancer drugs (25).…”

Section: Introductionmentioning

confidence: 99%

“…A growing body of data indicates that miR-335 plays an essential role in drug resistance (25)(26)(27). Kim et al found that miR-335/SIAH2/HDAC3 axis regulates the response to anticancer drugs (25). Another study revealed that the expression of miR-335 was downregulated in all the ovarian cancer resistant cells, suggesting a direct involvement in the development of chemoresistance (26).…”

Section: Introductionmentioning

confidence: 99%

N-peptide of vMIP-II reverses paclitaxel-resistance by regulating miRNA-335 in breast cancer

Wang

Ding

et al. 2017

International Journal of Oncology

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Acquisition of resistance to paclitaxel is one of the most important problems in treatment of breast cancer patients, but the molecular mechanisms underlying sensitivity to paclitaxel remains elusive. Emerging evidence has demonstrated that microRNAs (miRNAs) play important roles in regulation of cell growth, migration and invasion through inhibiting the expression of its target genes. In our previous studies, we have shown that microRNA-335 (miR‑335) decreased obviously between paclitaxel-resistant (PR) and parental breast cancer cells through miRNA microarray. However, the roles of miR‑335 in breast cancer progression and metastasis are still largely unknown. NT21MP was designed and synthesized as an antagonist with CXCR4 to inhibit cellular proliferation and induce apoptosis. Therefore, the aim of this study was to explore the underlying mechanism of miR‑335 and NT21MP in reverse PR in breast cancer cells. In this study, we found that miR‑335 expression is significantly lower in PR MCF‑7 and SKBR-3 cells (MCF‑7/PR and SKBR-3/PR) compared with their parental MCF‑7 and SKBR-3 cells. Functional experiments showed that overexpression of miR‑335 and NT21MP increased the number of apoptosis cells, arrested cells in G0/G1 phase transition, and suppressed cell migration and invasion in vitro. Dual luciferase assays revealed that SETD8 is a direct target gene of miR‑335. Furthermore, miR‑335 markedly inhibited expression of SETD8 via Wnt/β‑catenin signaling and subsequently inhibited the expression of its downstream genes cyclin D1, and c‑Myc. Additionally, ectopic expression of miR‑335 or depletion of its target gene SETD8 could enhance the sensitivity of PR cells to paclitaxel. Taken together, these date elucidated that NT21MP and miR‑335 mediated PR of breast cancer cells partly through regulation of Wnt/β‑catenin signaling pathway. Activation of miR‑335 or inactivation of SETD8 could be a novel approach for the treatment of breast cancer.

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“…The expression level of HDAC3 has been shown to be down-regulated in various cancer cell lines that are resistant to anti-cancer drugs ( Kim et al, 2014 ). The expression of HDAC3 is controlled via ubiquitination ( Kim et al, 2015b ). miR-335 increases the expression of HDAC3 by preventing SIAH2 from inducing ubiquitination of HDAC3 ( Kim et al, 2015b ).…”

Section: Introductionmentioning

confidence: 99%

“…The expression of HDAC3 is controlled via ubiquitination ( Kim et al, 2015b ). miR-335 increases the expression of HDAC3 by preventing SIAH2 from inducing ubiquitination of HDAC3 ( Kim et al, 2015b ). The selective inhibition of HDAC3 protects beta cells from cytokine-induced apoptosis ( El-Khoury et al, 2007 ).…”

Section: Introductionmentioning

confidence: 99%

Histone Deacetylase-3/CAGE Axis Targets EGFR Signaling and Regulates the Response to Anti-Cancer Drugs

Kim

Goh

et al. 2016

Molecules and Cells

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We have previously reported the role of miR-326-HDAC3 loop in anti-cancer drug-resistance. CAGE, a cancer/testis antigen, regulates the response to anti-cancer drug-resistance by forming a negative feedback loop with miR-200b. Studies investigating the relationship between CAGE and HDAC3 revealed that HDAC3 negatively regulated the expression of CAGE. ChIP assays demonstrated the binding of HDAC3 to the promoter sequences of CAGE. However, CAGE did not affect the expression of HDAC3. We also found that EGFR signaling regulated the expressions of HDAC3 and CAGE. Anti-cancer drug-resistant cancer cell lines show an increased expression of pEGFRY845. HDAC3 was found to negatively regulate the expression of pEGFRY845. CAGE showed an interaction and co-localization with EGFR. It was seen that miR-326, a negative regulator of HDAC3, regulated the expression of CAGE, pEGFRY845, and the interaction between CAGE and EGFR. miR-326 inhibitor induced the binding of HDAC3 to the promoter sequences in anti-cancer drug-resistant Malme3MR cells, decreasing the tumorigenic potential of Malme3MR cells in a manner associated with its effect on the expression of HDAC3, CAGE and pEGFRY845. The down-regulation of HDAC3 enhanced the tumorigenic, angiogenic and invasion potential of the anti-cancer drug-sensitive Malme3M cells in CAGE-dependent manner. Studies revealed that PKCδ was responsible for the increased expression of pEGFRY845 and CAGE in Malme3MR cells. CAGE showed an interaction with PKCδ in Malme3MR cells. Our results show that HDAC3-CAGE axis can be employed as a target for overcoming resistance to EGFR inhibitors.

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miR-335 Targets SIAH2 and Confers Sensitivity to Anti-Cancer Drugs by Increasing the Expression of HDAC3

Cited by 32 publications

References 58 publications

Inferences of individual drug responses across diverse cancer types using a novel competing endogenous RNA network

Inferences of individual drug responses across diverse cancer types using a novel competing endogenous RNA network

N-peptide of vMIP-II reverses paclitaxel-resistance by regulating miRNA-335 in breast cancer

Histone Deacetylase-3/CAGE Axis Targets EGFR Signaling and Regulates the Response to Anti-Cancer Drugs

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